In a recent breakthrough, Professor Wang Qi's research team at the School of Biological Engineering, East China University of Science and Technology, has made significant strides in understanding the regulation of pathogen virulence. Their findings were published in "Nucleic Acids Research."
If we liken the core genome of bacteria to indigenous inhabitants within a bacterial community, then the primary driving force behind bacterial evolution is the continual fusion of horizontal gene transfer elements (invaders) with the indigenous population, thereby endowing or enhancing traits such as bacterial pathogenicity and environmental adaptability. The Type III secretion system (T3SS), Type VI secretion system (T6SS), resistance genes, and prophages are typical "invaders" capable of propelling ordinary bacteria towards becoming pathogens. Simultaneously, the expression fusion of these "invaders" can encroach upon the survival resources of the "indigenous inhabitants," prompting the deployment of guardians—such as the H-NS-like nucleoid-associated proteins—to silence the expression of invaders.
Building upon previous research, the team focused on the model pathogen Edwardsiella piscicida within the Enterobacteriaceae family. They discovered that lysine acetylation modification influences H-NS-mediated silencing of T3/T6SS, indicating lysine acetylation as a mechanism resistant to H-NS silencing. E. piscicida responds to changes in amino acid nutrition or immune metabolites levels in the environment by modulating the lysine acetylation modification status of H-NS. Particularly, acetylation at the K120 site significantly weakens H-NS's ability to occupy high-AT content DNA. These high-AT content DNA segments are mainly concentrated in the promoter regions of horizontal gene transfer elements, and H-NS, deprived of its occupancy capability, is more susceptible to expulsion by anti-silencing proteins, thereby completely alleviating the inhibition of T3/T6SS silencing.
Acetylation of lysine affects H-NS binding to high AT DNA. Image source: Nucleic Acids Research.
Related paper information: https://doi.org/10.1093/nar/gkad1172
